Recommendations for prevention and treatment of vitamin D deficiency rickets
Vit D deficiency rickets (rickets of vitamin D deficiency) (rickets for short) is a systemic chronic nutritional disease characterized by skeletal lesions during the growth period due to abnormal calcium and phosphorus metabolism in the body caused by Vit D deficiency, resulting in incomplete mineralization of bone tissue.
In view of the fact that rickets is mostly seen in infants and young children within 3 years of age, this recommendation focuses on rickets in infants and young children.
I. Prevention
(a) Prevention during pregnancy of mothers
Pregnant women should be active outdoors frequently and eat foods rich in calcium and phosphorus. Women in the second trimester of pregnancy are recommended to take VitD 400-1000 U/d (10-25μg/d) as appropriate. If available, pregnant women should have their blood 25-(OH)D concentrations monitored during the second trimester of pregnancy, and if there is significant VitD deficiency, VitD should be supplemented to maintain 25-(OH)D levels in the normal range. VitA,D preparations should be used to avoid VitA toxicity, VitA intake <10,000 U/d
(II ) Infants and children prevention
1. Outdoor activities: Parents should be instructed to take their infants outdoors as early as possible, gradually reaching 1-2 h/d, and exposing infants’ body parts such as head, face, hands and feet as much as possible.
VitD supplementation: Infants (including exclusively breastfed children) should receive 400 U/d (10 μg/d) of VitD 2 weeks after birth until 2 years of age. If infants consume 500m l of formula daily, they can take in about 200U (5μg) of VitD, and with appropriate outdoor activities (especially in summer when there are more outdoor activities), there is no need to supplement VitD preparations.
3, high-risk groups supplementation: premature infants, low birth weight infants, twins should be supplemented with VitD 800-1000 U/d (20-25μg/d) immediately after birth, and after 3 months to 400 U/d (10μg/d).
II. Diagnosis
(a) Risk factors for VitD deficiency
1. Insufficient storage during fetal life: The fetus obtains VitD from the mother through the placenta and stores it in the body to meet its needs for a period of time after birth.
2, lack of sunlight exposure: sunlight ultraviolet light can not pass through ordinary glass, infants and young children outdoor activities, VitD generation is insufficient; high-rise buildings block sunlight, atmospheric pollution (such as smoke, dust) can absorb part of the ultraviolet radiation; winter sunlight exposure reduced, affecting the skin synthesis of VitD.
3, insufficient intake: natural food VitD content is low, such as dairy (including human milk and cow and goat milk, etc.), poultry egg yolk, meat and other content is low, cereals, vegetables, fruits almost no VitD .
(B) Clinical manifestations
The clinical manifestations of rickets include non-specific symptoms, characteristic skeletal changes and other systemic changes.
The active phase of rickets is divided into early, radical, recovery and sequelae phases.
1.Early stage : Mostly seen in infants under 6 months old (especially under 3 months old). There may be non-specific neuropsychiatric symptoms such as excessive sweating, occipital baldness, irritability, and night terrors. There are often no skeletal lesions at this stage. Blood calcium and phosphorus are normal or slightly low, alkaline phosphatase (AKP) is normal or slightly high, and blood 25-(OH) D is decreased. There is no abnormality in the long bone x-ray or the temporary calcification zone is blurred and thinned, and the dry marrow end is slightly widened.
2, radical phase : Skeletal signs: <6 months old infant, cranial softening signs (ping-pong feeling) can be seen; >6 months old infant, square skull, hand (foot) bracelet, rib bead, rib cartilage groove, chicken chest, 0-shaped leg, X-shaped leg and other signs can be seen. Blood calcium is normally low or decreased, blood phosphorus is significantly decreased, and AKP is increased. Blood 25-(OH) D,1,25-(OH)2D was significantly decreased. Bone X-ray film widening of the medullary end of the long bone stem, disappearance of the temporary calcification zone, brush-like or cup-like, widening of the bone marrow cartilage disc >2 mm.
3.Recovery period :The symptoms disappear after sunlight exposure or treatment in early or active children, and the signs gradually reduce or disappear. Blood calcium, blood phosphorus, AKP, 25-(O H)D, 1,25-(OH)2D gradually return to normal. The temporary calcification zone at the dry end of the long bones on bone X-ray was reappeared, widened and increased in density, and the skeletal cartilage disc was <2 mm.
4. Posterior phase:Mostly seen in children after 3 years of age, due to severe rickets in infancy and childhood, different degrees of skeletal deformities can be left behind. Generally, there are no clinical symptoms and normal blood biochemical examination.
In addition to skeletal lesions, Vit D deficiency can also affect other tissues and organs, causing delayed motor development, such as muscle relaxation and reduced muscle strength (muscle tone); and decreased immune function recurrent infections. Vit D deficiency in children may be associated with certain chronic diseases in adulthood, such as diabetes, asthma, multiple sclerosis, etc.
Vit D deficiency risk factors, clinical signs and symptoms help in the diagnosis, and blood biochemistry and bone radiographs are needed to confirm the diagnosis. Serum 25-(OH)D is the best indicator of VitD nutritional status and should be carried out gradually.
(C) Differential diagnosis
Vit D deficiency rickets needs to be differentiated from other non-VitD deficiency rickets (e.g. renal osteotropic disorder, renal tubular acidosis, hypophosphatemic anti-VitD rickets, Fanconi syndrome), endocrine and bone metabolic diseases (e.g. hypothyroidism, chondrodysplasia, mucopolysaccharidosis), etc.
Children with chronic diarrhea or hepatobiliary or pancreatic diseases or taking anti-epileptic drugs can affect the absorption, metabolism, and transmutation of VitD in the body, resulting in secondary VitD deficiency, which also needs to be differentiated.
Treatment
(A) VitD treatment
The purpose of treatment is to control the disease and prevent skeletal deformities, the principle of treatment is mainly oral, VitD preparation selection, dose size, duration of treatment, single or multiple, route (oral or intramuscular injection) should be determined according to the specific circumstances of the child, emphasizing the individualized administration of drugs.
If oral administration is difficult or diarrhea affects the absorption, high-dose assault therapy can be used. After 1 month of medication, follow-up should be conducted, and if symptoms, signs and laboratory tests do not improve, other diseases should be considered and differential diagnosis should be paid attention to, while hypercalcemia, hypercalciuria and VitD overdose should be avoided.
(B) Other treatment
Calcium supplementation: Milk is a reliable source of calcium nutrition for infants and children, and calcium supplementation is generally not required for rickets treatment.
Micro-nutrient supplementation: attention should be paid to the intake of other multivitamins.
3.Surgery: Severe skeletal deformities can be surgically corrected.